By Robert Feil, Daniel Metzger
Leading specialists supply well timed and finished details on equipment for conditional mutagenesis within the mouse (part 1) and their program to version human body structure and pathophysiology (part 2). It illustrates how refined genetic manipulations of the mouse genome are hired to version human ailments and to spot underlying molecular mechanisms. eventually the booklet considers the improvement of latest medicines to regard them.
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Additional info for Conditional Mutagenesis: An Approach to Disease Models
EMBO Reports 2:292– 297 28 R. Feil Wang J, Wilhelmsson H, Graff C, Li H, Oldfors A, Rustin P, Bruning JC, Kahn CR, Clayton DA, Barsh GS, Thoren P, Larsson NG (1999) Dilated cardiomyopathy and atrioventricular conduction blocks induced by heart-speciﬁc inactivation of mitochondrial DNA gene expression. Nat Genet 21:133–137 Wen F, Cecena G, Munoz-Ritchie V, Fuchs E, Chambon P, Oshima RG (2003) Expression of conditional cre recombinase in epithelial tissues of transgenic mice. Genesis 35:100–106 Wolfsgruber W, Feil S, Brummer S, Kuppinger O, Hofmann F, Feil R (2003) A proatherogenic role for cGMP-dependent protein kinase in vascular smooth muscle cells.
Nat Genet 21:133–137 Wen F, Cecena G, Munoz-Ritchie V, Fuchs E, Chambon P, Oshima RG (2003) Expression of conditional cre recombinase in epithelial tissues of transgenic mice. Genesis 35:100–106 Wolfsgruber W, Feil S, Brummer S, Kuppinger O, Hofmann F, Feil R (2003) A proatherogenic role for cGMP-dependent protein kinase in vascular smooth muscle cells. Proc Natl Acad Sci U S A 100:13519–13524 Wood AJ, Darbyshire J (2006) Injury to research volunteers–the clinical-research nightmare. N Engl J Med 354:1869–1871 Wunderlich FT, Wildner H, Rajewsky K, Edenhofer F (2001) New variants of inducible Cre recombinase: a novel mutant of Cre-PR fusion protein exhibits enhanced sensitivity and an expanded range of inducibility.
1999). 2 and inducing cardiovascular, thymus and parathyroid defects as well as craniofacial anomalies and learning difﬁculties. The 24–30 genes deleted in DGS map in a single region in mouse chromosome 16. 2-Mb deletion between Es2 and Ufd1 in mouse chromosome 16, displayed a panel of abnormalities reminiscent of those found in human patients. Other mouse models were subsequently produced in order to decipher the genes involved in DGS. Puech et al. (2000) generated a new deletion partially overlapping with the Df1 deletion.